The three dimensional spatial variations in the cooling pattern of the Toki granitic body, a zoned pluton in Central Japan, have been evaluated quantitatively by thermochronology using cooling age determination based on the different closure temperatures for target mineral species. The Toki granite has hornblende K-Ar ages of about 74.3±3.7 Ma (n = 2; closure temperature of 510±25 o C), biotite K-Ar ages of 78.5±3.9 to 59.7±1.5 Ma (n = 33; 300±50 o C), and zircon fission-track ages of 75.6 ±3.3 to 52.8±2.6 Ma (n = 44; 240±50 o C).The spatial variation in the biotite K-Ar age is similar to that in the zircon fission-track age in samples collected from 11 boreholes and seven outcrop sites in the Toki granite, indicating that cooling was effectively from the roof and also from the northwest margin. This cooling pattern shows a strong correlation with the Alumina Saturation Index (ASI) distribution of the body.Larger ASI values correspond to earlier and more rapid cooling after emplacement and smaller value to slower cooling. Toki granite was effectively cooled from the peraluminous regions where assimilation of country sedimentary rock was most extensive.
We report a case of a 32-year-old male, an asymptomatic carrier of human T-cell leukemia virus type 1 (HTLV-1), who underwent a renal transplantation and developed adult T-cell leukemia (ATL) during the course of posttransplant immunosuppressive treatment. He was treated with combination chemotherapies consisting of cyclophosphamide, vincristine, doxorubicin, prednisolone, cisplatin, cytosine arabinoside, etoposide, and methyl-prednisolone, without any improvement. Bestrabucil (KM2210), a conjugate of chlorambucil and estradiol, was administered as an alternative therapy; this therapy successfully suppressed his leukemic cell growth, and partial remission was achieved. Posttransplant immunosuppressive therapy with prednisolone, mizoribine, and cyclosporin A might have been the predominant cause of the transition from an asymptomatic HTLV-1 infection to overt ATL. A careful approach is required with HTLV-1 asymptomatic carriers who need organ transplantation followed by immunosuppressive treatment.
Summary
Aberrant DNA methylation is frequently observed in adults with myelodysplastic syndrome (MDS), and is recognized as a critical event in the disease's pathogenesis and progression. This is the first report to investigate the methylation status of p15 and p16, cell cycle regulatory genes, in children with MDS (n = 9) and juvenile myelomonocytic leukaemia (JMML; n = 18) by using a methylation‐specific polymerase chain reaction. The frequency of p15 hypermethylation in paediatric MDS was 78% (7/9), which was comparable to that in adult MDS. In contrast, p15 hypermethylation in JMML was a rare event (17%; 3/18). In JMML, clinical and laboratory characteristics including PTPN11 mutations and aberrant colony formation were not different between the three patients with hypermethylated p15 and the others. Aberrant methylation of p16 was not detected in children with either MDS or JMML. Since p15 and p16 genes were unmethylated in two children with JMML, in whom the disease had progressed with an increased number of blasts, a condition referred to as blastic crisis, we infer that the aberrant methylation of these genes is not responsible for the progression of JMML. The results suggest that demethylating agents may be effective in most children with MDS and a few patients with JMML.
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